Rats will decrease intake of a saccharin conditioned stimulus (CS) following pairing with an illness-inducing agent such as LiCl, a preferred high concentration of sucrose, or a drug of abuse such as morphine or cocaine. The suppressive effects of the illness-inducing agent are clear evidence for aversive conditioning and are referred to as conditioned taste aversions. The suppressive effects of the rewarding sucrose solution reflect appetitive conditioning and are referred to as anticipatory contrast effects because the saccharin CS is thought to be devalued as it comes to predict the future availability of the preferred sucrose reward. Finally, despite the well-known rewarding properties of drugs of abuse, the suppressive effects of these drugs have been viewed as conditioned taste aversions for over 25 years. We have, however, recently posed an alternative interpretation that eliminates this apparent paradox. Specifically, we have suggested that rats suppress intake of a saccharin CS following saccharin-morphine pairings, for example, because the saccharin CS is devalued as it comes to predict the future availability of the highly rewarding drug of abuse. Thus, we postulate that the same rewarding properties that increase self-administration of the drug also serve to devalue the gustatory cue that predicts its availability. The results from the Preliminary Studies support this novel hypothesis by showing that the suppressive effects of drugs of abuse and sucrose, but not LiCl, are influenced by deprivation state of the animal, the caloric value of the gustatory CS, the strain of the rat, and lesions of the gustatory thalamus. The objective of this proposal is to use a lesion-behavioral analysis to (I) evaluate the relative contribution of the gustatory thalamus and its terminal projection region, the gustatory cortex, (II) identify the parametric constraints on the impairment, and (III), given that rats will suppress saccharin intake when paired with iv cocaine (Preliminary Study #5), examine the nature of the lesion-induced deficit using the self-administration task.